New Evidence of Exercise Training Benefits in Myostatin-Deficient Mice: Effect on Lipidomic Abnormalities
Open accessAbstract
Myostatin ( Mstn ) inactivation or inhibition is considered as a promising treatment for various muscle-wasting disorders because it promotes muscle growth. However, myostatin-deficient hypertrophic muscles show strong fatigability associated with abnormal mitochondria and lipid metabolism . Here, we investigated whether endurance training could improve lipid metabolism and mitochondrial membrane lipid composition in mice where the Mstn gene was genetically ablated ( Mstn −/- mice). In Mstn −/- mice , 4 weeks of daily running exercise sessions (65–70% of the maximal aerobic speed for 1 h) improved significantly aerobic performance, particularly the endurance capacity (up to +280% compared with untrained Mstn −/- mice), to levels comparable to those of trained wild type (WT) littermates. The expression of oxidative and lipid metabolism markers also was increased, as indicated by the upregulation of the Cpt1 , Ppar-δ and Fasn genes. Moreover, endurance training also increased, but far less than WT, citrate synthase level and mitochondrial protein content. Interestingly endurance training normalized the cardiolipin fraction in the mitochondrial membrane of Mstn −/- muscle compared with WT. These results suggest that the combination of myostatin inhibition and endurance training could increase the muscle mass while preserving the physical performance with specific effects on cardiolipin and lipid-related pathways.
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Myostatin deficiency alters cardiolipin composition within mitochondrial membrane, changes that can be partially reversed through endurance training.
“Additionally, it alters cardiolipin composition within the mitochondrial membrane, changes that can be partially reversed through endurance training [74].”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [74]
Despite these deficits, myostatin deficiency enhances basal oxygen consumption, reduces lipid peroxidation, and upregulates glutathione antioxidant system.
“Despite these deficits, myostatin deficiency enhances basal oxygen consumption, reduces lipid peroxidation, and upregulates the glutathione antioxidant system.”
From Exercise-Induced Muscle–Fat Crosstalk: Molecular Mediators and Their Pharmacological Modulation for the Maintenance of Metabolic Flexibility in Aging (2025) · cites this paper as [74]
The Introduction describes aerobic metabolic deficits in myostatin-deficient mice, and the section on muscle lipid metabolism discusses reduced mitochondrial cardiolipin. Neither passage addresses enhanced basal oxygen consumption, reduced lipid peroxidation, or upregulation of the glutathione antioxidant system; searches for those terms found no supporting passage in our copy. (LLM, conf=0.76)
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- Authors
- Baati, N., Feillet-Coudray, C., Fouret, G., Vernus, B., Goustard, B., Jollet, M., Bertrand-Gaday, C., Coudray, C., Lecomte, J., Bonnieu, A., & Koechlin-Ramonatxo, C.
- Affiliations
- Université de Montpellier (FR)
- Centre de Coopération Internationale en Recherche Agronomique pour le Développement (FR)
- Venue
- Biochemical and Biophysical Research Communications
- Publisher
- Elsevier BV
- Published
- 2019-08
- Volume
- 516
- Issue
- 1
- Pages
- 89-95
- ISSN
- 0006-291X (ISSN-L)
- OpenAlex
- W2953288471
- Cited by
- 15
- References
- 30
- Citations by year
- 2025: 2 · 2024: 1 · 2023: 2 · 2022: 3 · 2021: 2 · 2020: 4 · 2019: 1
- FWCI
- 0.83
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Biochemical and Biophysical Research Communications (acceptedVersion, other-oa)
- PubMed (publishedVersion)
- HAL (submittedVersion, cc-by-nc)
- Agritrop (Cirad) (submittedVersion, cc-by-nc)
- Funders
- Centre de Coopération Internationale en Recherche Agronomique pour le Développement (UMR IATE,F-34398)
- Université de Montpellier
- Institut National de la Recherche Agronomique
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
- Keywords
- myostatin, Mstn knockout mice, endurance training, lipid metabolism, mitochondrial membrane lipids, cardiolipin, lipidomics, muscle fatigue, muscle hypertrophy, aerobic performance, citrate synthase, PPARδ, carnitine palmitoyltransferase 1, fatty acid synthase, mitochondrial dysfunction
- MeSH terms
- Lipidomics, Animals, Male, Physical Conditioning, Animal, Physical Endurance, Running, Gene Deletion, Mice, Knockout, Lipid Metabolism, Mice, Myostatin
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